M5. Beta Amyloid Level is not Elevated in Elderly Patients With Schizophrenia: Are There Potential Neuroprotective Effects of Antipsychotics on Beta-Amyloid Pathology?
Bibliographic record
Abstract
Background: Current literature suggests that the pathology of schizophrenia (SCZ) has developmental origins based on mounting evidence showing genetic abnormalities and prenatal factors contributing to the early onset of the illness. Nonetheless, there are progressive neurodegenerative processes in this illness that cannot be solely explicated by the neurodevelopmental theory of SCZ. In addition, numerous animal studies showed that antipsychotics elicit neuroprotective effects by lowering beta-amyloid (Aβ) levels. Methods: Focusing on beta-amyloid (Aβ) as a measure of neurodegenerative changes, a systemic review and meta-analysis investigating Aβ in SCZ and the link between antipsychotic usage and Aβ was conducted. A literature search using PsychINFO, Medline and Embase was carried out, examining studies that compared Aβ between patients with SCZ and comparison groups. Results: Among 14 identified studies, there were 11 studies comparing Aβ between SCZ and elderly controls, and 7 studies comparing Aβ between SCZ and AD. Meta-analysis showed that Aβ levels did not differ in patients with SCZ from controls. Patients with SCZ showed attenuated level of Aβ in comparison to patients with AD. Subsequently, only 1 of 5 studies in the sub-analysis showed a correlation between the duration of antipsychotic usage and decreased level of Aβ, while the other 4 studies highlighted no link between the duration of antipsychotic usage and Aβ. Conclusion: In conclusion, Aβ level is not increased in SCZ in comparison to controls and AD. Unlike the animal literature, the relationship between antipsychotic exposure and Aβ in SCZ remains elusive. Limitations include small sample sizes, different techniques to quantify Aβ and investigation of different cortical regions. Future studies should examine other neurodegenerative markers in SCZ, including oxidative stress and apoptosis dysregulation to better elucidate the pathophysiological mechanisms underlying this illness.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.003 | 0.010 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.002 | 0.002 |
| Bibliometrics | 0.002 | 0.002 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.002 | 0.001 |
| Insufficient payload (model declined to judge) | 0.007 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".